脑动静脉畸形导致出血的多层螺旋CT血管造影的相关因素分析

目的 探讨多层螺旋CT血管成像(MSCTA)显示脑动静脉畸形(AVM)合并出血的影像学相关因素.方法 通过比较脑AVM出血组和未出血组之间MSCTA所显示的供血动脉、畸形血管团、引流静脉特点.结果 脑出血组与未出血组两组间MSCTA所显示得畸形血管团部位、大小、引流静脉条数、引流静脉是否受损以及有无合并动脉瘤比率差异有统计学意义.结论 MSCTA提示导致AVM的血管压力增高的深部位、小病灶、单支引流静脉或引流静脉狭窄、闭塞以及合并动脉瘤是脑AVM合并出血的密切相关因素.MSCTA为临床治疗提供依据和借鉴.     

MSCTA在自发性蛛网膜下腔出血超急性期诊疗中的应用

目的探讨多排螺旋CT三维血管成像（MSCTA）在自发性蛛网膜下腔出血（SAH）超急性期诊疗中的作用、评价MSCTA在SAH患者病因诊断学中的价值。方法回顾分析经CT平扫及腰穿明确诊断的自发性蛛网膜下腔出血48例患者，在超急性期（24h内）行多排螺旋CT血管造影检查，并与DSA全脑动脉造影检查比较。结果48例患者中MSCTA发现动脉瘤34例，显示瘤体、瘤颈、载瘤动脉和与周围血管及颅骨的关系清晰、确切；动静脉畸型（AVM）7例，显示畸形血管团的部位、大小、供血动脉来源，引流静脉的分支情况，空间立体结构清晰。颈内动脉海绵窦瘘（ICCF）1例，显示扩张的海绵窦大小、形态、范围及纡曲的引流静脉，可显示ICCF的瘘口；静脉性血管畸形（CVM）3例；不明原因3例。对脑血管病的检出敏感性为95％，特异性为100％。结论MSCTA是简单、快速、无创、安全、可靠的脑血管成像技术，在一定程度上可替代DSA检查，可作为sAH超急性期患者病因诊断的首选检查方法。     

脑动静脉畸形与血流动力性动脉瘤相关性研究

目的 探索与血流动力性动脉瘤有统计学相关性的脑动静脉畸形(AVM)特征性因素.方法 对1999年8月至2009年7月363例AVM患者的资料进行回顾性统计分析;其中男性229例,女性137例,年龄5～65岁,平均(28±13)岁.采用SPSS 16.0统计软件对AVM的13个特征性因素与合并血流动力性动脉瘤之间进行单因素与多因素的相关性分析,对筛选出的因素进行评估.结果 单因素分析表明:与血流动力性动脉瘤存在统计学相关性的因素为发病年龄、部位(幕上、幕下)、AVM的大小、主干供血动脉根数、引流静脉根数、引流静脉扩张、对侧供血、前后循环同时供血.多因素分析表明:发病年龄、主干供血动脉根数、对侧供血与血流动力性动脉瘤存在统计学意义的正相关性,引流静脉根数与血流动力性动脉瘤存在统计学意义的负相关性.结论 与血流动力性动脉瘤相关的AVM特征性因素为发病年龄、主干供血动脉根数、引流静脉根数、对侧供血.     

脑动静脉畸形伴发动脉瘤的出血风险因素分析及介入治疗

目的探讨脑动静脉畸形伴发动脉瘤出血风险因素及介入治疗策略。方法收集并整理42例脑动静脉畸形伴发动脉瘤患者的临床和影像学资料。根据患者术中造影结果,分析脑动静脉畸形血管特点,制定相应介入栓塞治疗方案。术后3个月、6个月及1年分别复查DSA,明确病灶有无复发。结果病灶位于幕下、由深静脉引流或混合静脉引流、Spetzler-Martin分级Ⅲ~Ⅳ以及Redekop分型Ⅰ型和Ⅱa型动脉瘤患者易出血。38例介入治疗后经康复治疗后格拉斯哥结果评分4分,1例视力受损,2例有不同程度肢体功能障碍,1例死亡。随访复查37例,均无动静脉畸形复发,且动脉瘤栓塞良好。结论术前明确血管构筑特点及潜在出血风险因素并制定个体化治疗方案,有助于提高介入栓塞治疗脑动静脉畸形伴发动脉瘤的安全性和有效性。     

Galen静脉动脉瘤样畸形血管影像学分类和治疗

Ｇａｌｅｎ静脉动脉瘤样畸形是一种少见的颅内血管畸形，由于位置深在，治疗较为困难。作者收治１１例该类畸形，其中５例为先天性Ｇａｌｅｎ静脉动脉瘤样畸形（ＶＧＡＭ），治疗主要是闭塞瘘口；继发性Ｇａｌｅｎ静脉动脉瘤样扩张（ＶＧＡＤ）５例，其治疗主要是栓塞脑实质或硬膜的畸形血管来达到治愈或改善临床症状；另１例依据ＭＲＩ进行诊断，未作造影及分类。本组有８例行血管内治疗，其中５例治愈，３例临床症状好转；有２例发生自发血栓，未治疗。作者对Ｇａｌｅｎ静脉动脉瘤样畸形的概念、分类及影像学特点，特别是血管内治疗方法和注意事项进行了讨论。     

脑动静脉畸形出血的危险因素

目的探讨脑动静脉畸形(BAVM)出血的危险因素。方法收集DSA确诊的BAVM患者105例,分析BAVM出血的危险因素。结果单因素分析表明,BAVM破裂出血的危险因素有病灶位置、大小,供血动脉类型、数目,引流静脉类型、数目、形态及是否合并动静脉瘘;多因素Logistic分析发现,病灶位置、大小,供血动脉类型、数目,引流静脉数目及是否合并动静脉瘘是出血的危险因素,而引流静脉扩张可能是保护因素。结论病灶位于幕下或大脑深部、畸形团3cm、单支静脉引流、单纯穿支动脉供血及多支供血动脉、合并动静脉瘘是BAVM出血的危险因素。     

脑动静脉畸形合并畸形团外囊性动脉瘤六例

我科自2001年1月～2002年12月共收治脑动静脉畸形(arteriovenous malformation，AVM)合并畸形团外囊性动脉瘤6例，占同期69例脑AVM的8．7％，同期103例脑动脉瘤的5．8％，现报告如下。     

脑动静脉畸形并出血的显微手术治疗

目的 回顾性分析78例脑动静脉畸形（AVM）并出血的显微外科手术治疗结果，探讨AVM并出血的显微手术技巧及适应证。方法 所有病例术前均接受CT检查，术后均接受CT及MRI检查，其中25例接受了DSA检查。所有病例均在全麻状态下进行显微外科手术治疗，少部分AVM未能全切的病例，术后用γ-刀或血管内介入治疗。结果 血肿全清除69例，大部分清除9例；AVM全切除70例，8例部分切除或未能切除，加用γ-刀或血管内介入治疗。手术后死亡6例（8．0％），偏瘫4例（5．1％），失语2例（2．6％），偏盲1例（1．3％），脑神经功能障碍4例（5．1％），无颅内感染。结论 应用显微外科手术治疗脑AVM并出血安全有效，而且并发症、后遗症较少，应成为脑AVM并出血患者治疗的最佳选择，对特殊位置的AVM，不宜强行切除，手术时只作血肿清除，术后加用γ-刀或血管内介入治疗。     

术中ICG荧光血管造影在出血性脑动静脉畸形切除术中的应用体会

目的 研究术中吲哚菁绿（ICG）荧光血管造影在出血性脑动静脉畸形切除术中的应用价值。方法 回顾性分析2010年1月至2021年12月我院收治的8例出血性脑动静脉畸形行开颅手术患者的术中ICG荧光造影、术前CTA及术后DSA血管影像资料。对比术中ICG荧光血管影像与术前CTA、术后DSA血管影像,评估ICG荧光血管造影在术中的作用。结果 8例患者血管畸形团在术中ICG荧光血管造影均显影清晰;供血动脉及引流静脉影像与术前CTA血管影像一致;切除术后ICG荧光血管造影血管畸形团均未显影,与术后DSA血管影像一致。结论 术中ICG荧光血管造影可以显示血管畸形团范围,明确供血动脉及引流静脉,在出血性脑动静脉畸形切除术中有指导意义。     

多层螺旋CT血管造影对于外科处理脑动脉瘤蛛网膜下腔出血的指导作用和临床经验

目的研究多层螺旋CT血管造影(MSCTA)诊断脑动脉瘤的临床应用。方法选择我院2014年10月~2017年1月收治的60例蛛网膜下腔出血疑似脑动脉瘤患者进行的MSCTA检查的临床资料,其中15例行保守治疗;其余45例行MSCTA患者经过外科处理,包括41例经DSA血管内处理,4例经开颅手术治疗。分析CTA的诊断准确性、应用价值和作者的使用经验。结果CTA:所有患者中45例MSCTA诊断脑动脉瘤共47个,DSA及开颅术发现脑动脉瘤49个,诊断符合率为95.9%;CTA与DSA对瘤体长轴、瘤体短轴与瘤颈进行分析显示,两种检测方法的检测数据均无明显差异,P0.05。结论对于颅内动脉瘤患者采取MSCTA检测的临床意义重要,有利于显示出患者颅内动脉瘤的瘤体大小与瘤颈,诊断方法安全、可靠。     

Venous malformation serving as the draining vein of an adjoining arteriovenous malformation. Case report and review of the literature

BACKGROUND: Widely accepted pathologic classification of venous malformations includes discrete venous, arteriovenous, capillary, and cavernous malformations, each with distinct pathological criteria for definition. Several authors have described mixed or transitional vascular malformations with pathological features of more than one type of malformation within the same lesion. We present a rare case of a venous malformation associated with an arteriovenous malformation (AVM). CASE DESCRIPTION: A 37-year-old woman presented with a loss of consciousness. Computed tomography showed an enlarged vein running along the lateral wall of the right lateral ventricle. A cerebral angiogram demonstrated an AVM and a venous malformation in the right hemisphere; the AVM and the venous malformation were located in proximity to each other with the AVM using the venous malformation as its draining vein. In this case, where an AVM used the venous malformation as the draining vein, only the AVM was treated by proton-beam radiosurgery. Follow-up magnetic resonance angiography demonstrated complete obliteration of the AVM with the venous malformation remaining unchanged. CONCLUSION: Arteriovenous shunting would have disturbed venous drainage resulting in the development of the venous malformation. Thus, in addition to demonstrating a rare coexistence of AVM and venous malformation, this case also offers a new insight into the pathogenesis of these vascular malformations.     

An analysis of the venous drainage system as a factor in hemorrhage from arteriovenous malformations.

The authors studied the venous drainage system and its impairment in relation to risk of hemorrhage in 108 cases of supratentorial arteriovenous malformation (AVM). The proportion of AVM's undergoing hemorrhage (hemorrhagic rate) was calculated in relation to: 1) the number of draining veins (one, two, or three or more); 2) the presence or absence of impairment in venous drainage (severe stenosis or occlusion in draining veins); and 3) the location of draining veins (deep venous drainage alone, superficial venous drainage alone, or a combination of the two). Statistical analysis demonstrated that AVM's with the following characteristics had a high risk of hemorrhage: 1) one draining vein (hemorrhagic rate 89% in 54 patients); 2) severely impaired venous drainage (hemorrhagic rate 94% in 18 patients); and 3) deep venous drainage alone (hemorrhagic rate 94% in 32 patients). The present study suggests that the venous drainage system of AVM's is significantly associated with the risk of hemorrhage of these lesions. Therefore, careful preoperative angiographic evaluation of the venous drainage system is mandatory for decision making in the management of patients with AVM's.     

Diffuse arteriovenous malformations: a clinical, radiological, and pathological description.

In a review of our series of patients with arteriovenous malformations (AVMs), a group with atypical angiographic and histopathological characteristics was discovered. Unlike the typical AVM, these lesions contained normal cerebral tissue between the abnormal vessels. We call these lesions diffuse AVMs, and think that this AVM represents one end of the AVM spectrum from a tight nidus to a diffuse lesion. The mean age of these patients was 18.1 years. Eight patients presented with an intracerebral hemorrhage, two with seizures, one with headache without hemorrhage, and one with ischemic symptoms compatible with vascular steal. Cerebral angiography revealed three AVMs to be 2 to 4 cm in diameter, four were 4 to 6 cm in diameter, and five were > 6 cm in diameter. Characteristic angiographic features included multiple small arterial feeders, small ectatic vessels in the malformation itself, multiple small draining veins, and a diffuse, puddling appearance of the contrast dye. Despite 16 operations in 11 patients, complete resection of the AVM was accomplished in only 8. The four patients with residual disease have received radiation therapy. Histopathology of the surgical specimens found AVM vessels interspersed among normal appearing neurons and white matter. Leptomeningeal angiodysplasia was noted when the cerebral cortex was involved. Gliosis was noted in some cases. Diffuse AVMs represent a difficult surgical challenge and recognition of the lesion aids in surgical planning.     

A case of cerebral arteriovenous malformation revealed at repeated subcortical hematoma with initially normal angiogram]

An 18-year-old male admitted to our hospital suffered left temporal subcortical hemorrhage. No abnormality was demonstrated on carotid or vertebral angiography at that time. On the day following the onset, left frontotemporal craniotomy was performed and the subcortical hematoma was evacuated. No vascular malformation was found despite careful investigation. On 30th day after the onset, the repeat cerebral angiography was performed but failed to show any vascular abnormalities. After discharge he was in good health, and had had some follow up, CT were normal except for the hematoma cavity. Just two years after the first operation he suffered a second left temporal hemorrhage. Cerebral angiography was repeated and a temporal arteriovenous malformation (AVM) was found with feeding vessels from the M-1 and M-2 portion of the left middle cerebral artery and from the left anterior choroidal artery, and draining veins to vein of Rosenthal and the straight sinus. One month after the second hemorrhage, left frontotemporal craniotomy was performed and complete excision of the AVM was carried out. Only five cases of AVMs in patients with normal angiograms several years before have been reported previously in the literature. But there are no cases in which surgery has been performed. Differently to those cases, in this case it was investigated operatively whether there was a vascular abnormality at the first hemorrhage. We didn't think, however, that the AVM demonstrated at the second hemorrhage had developed spontaneously because there had been a hemorrhage of unknown origin previous to it. It was assumed that a small angiographically occult AVM connected to the hematoma cavity existed at the time of the first hemorrhage but it was too small to be found even during surgical procedure. Such an angiography occult AVM had been growing for two years, and its growth had probably been facilitated by the presence of the hematoma cavity left after the first operation.     

Ruptured supratentorial arteriovenous malformations associated with venous aneurysms

Summary Six patients with ruptured supratentorial arteriovenous malformation (AVM) and an associated venous aneurysm (ectasia, dilatation, varix, pouch) are described.At presentation, patients ranged in age from 16 to 61 years and were equally distributed according to sex. Maximal AVM diameter was between 2.5 and 5.0 cm at presentation while the maximal size of the venous aneurysm ranged between 0.75 and 3.0 cm. One patient had multiple venous pouches while 5 patients had a single venous aneurysm. Three patients had a single bleed; 1 patient had 2 bleeds; and 2 patients had 3 bleeds. Hemorrhage around the venous aneurysm was seen in 4 of 5 patients who underwent magnetic resonance imaging of the brain. One patient, who suffered 3 bleeds over a several year period, had both an increase in the size of the venous aneurysm as well as enlargement of the AVM. The following features did not appear to influence hemorrhage: AVM size or location; venous aneurysm size or location; age; sex; pattern; location or number of draining veins; or external circulation feeders.These observations suggest that a venous aneurysm may increase the risk of hemorrhage from a supratentorial AVM and may be an ominous feature.     

Stenotic and occlusive disease of the venous drainage system of deep brain AVM's

Angiograms obtained prior to treatment in 53 cases of deep-seated cerebral arteriovenous malformations (AVM's) were retrospectively analyzed with particular attention to the topography of the AVM nidus and the venous drainage. The location of the lesion was determined by a combination of angiography and computerized tomography. Twenty-seven AVM's involved the basal ganglia and thalamus, 12 were located in the corpus callosum, six were intraventricular, and eight involved the mesencephalon and brain stem. Forty-one patients (77.3%) presented with intracranial hemorrhage. Vessel wall irregularities and/or stenosis of the system of the vein of Galen were observed in 14 cases, and occlusion of the deep venous system was present in seven cases. These AVM's showed numerous collateral venous pathways through enlarged medullary and cortical regional veins. There was dominant participation of the basal vein of Rosenthal in all cases. Unique local hemodynamic factors produced by the convergence of the draining veins of the AVM's into the vein of Galen and straight sinus may lead to a higher incidence of stenosis and/or occlusion of the venous drainage. The relatively high incidence of intracranial hemorrhage in these deep-seated AVM's may suggest a relationship between an increased incidence of intracranial bleeding and impaired venous outlets.     

Hemorrhagic venous infarction after excision of an arteriovenous malformation: case report

A case of arteriovenous malformation (AVM) in which postoperative hemorrhagic infarction developed, probably because of occlusion of the former draining veins, is reported. The hemorrhage developed in the temporal lobe 3 days after the initial operation and was located in the immediate vicinity of the site of the AVM. The following findings suggest that the postsurgical hemorrhage probably resulted from a venous thrombosis: 1) no evidence of residual AVM; 2) delayed onset of the hemorrhage, inconsistent with the time course of a hemorrhage developing according to the breakthrough theory or with insufficient hemostasis with a high-pressure afterload; 3) good correlation between the location of the hemorrhage and the occlusion of the draining veins; and 4) multifocal hemorrhage affecting both the gray matter and the subcortical white matter. Postoperative hemorrhagic infarction caused by thrombosis in the draining veins is rare, but it should be considered as a distinct postoperative complication after removal of an AVM.     

Dural arteriovenous malformation associated with recurrent subdural haematoma and intracranial hypertension

An unusual case of intracranial hypertension and symptoms of a left parieto-occipital mass lesion due to a dural arteriovenous malformation (AVM) with a large and dilated draining vein is reported. The patient also had a history of homolateral recurrent subdural haematoma, 11 years before. Subdural haematoma is rarely associated to a dural AVM. We suggest that the recurrent subdural haematoma was due to the very slow and intermittent venous bleeding from the preexisting dural malformation, which progressively enlarged in the following years to become very large. The symptoms of intracranial hypertension and papilloedema may be explained by the increased pressure in the dural sinus and the cerebral venous system. On the other hand, focal neurological symptoms in our case resulted from the mass effect due to an aneurysmally dilated draining vein in the left parieto-occipital region.